miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.
Oxidative stress has been shown to contribute to the development of age-related macular degeneration (AMD). MicroRNAs (miRNA) are small non-coding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression. We showed miR-17-3p to be elevated in macular RPE ce...
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doaj-21db63b9db254049b45e382e8b0cba042020-11-25T00:08:36ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-01118e016088710.1371/journal.pone.0160887miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.Bo TianDaniel E MaidanaBernard DibJohn B MillerPeggy BouzikaJoan W MillerDemetrios G VavvasHaijiang LinOxidative stress has been shown to contribute to the development of age-related macular degeneration (AMD). MicroRNAs (miRNA) are small non-coding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression. We showed miR-17-3p to be elevated in macular RPE cells from AMD patients and in ARPE-19 cells under oxidative stress. Transfection of miR-17-3p mimic in ARPE-19 induced cell death and exacerbated oxidative lethality that was alleviated by miR-17-3p inhibitor. The expression of antioxidant enzymes manganese superoxide dismutase (MnSOD) and thioredoxin reductase-2 (TrxR2) were suppressed by miR-17-3p mimic and reversed by miR-17-3p inhibitor. These results suggest miR-17-3p aggravates oxidative damage-induced cell death in human RPE cells, while miR-17-3p inhibitor acts as a potential protector against oxidative stress by regulating the expression of antioxidant enzymes.http://europepmc.org/articles/PMC4978424?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Bo Tian Daniel E Maidana Bernard Dib John B Miller Peggy Bouzika Joan W Miller Demetrios G Vavvas Haijiang Lin |
spellingShingle |
Bo Tian Daniel E Maidana Bernard Dib John B Miller Peggy Bouzika Joan W Miller Demetrios G Vavvas Haijiang Lin miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells. PLoS ONE |
author_facet |
Bo Tian Daniel E Maidana Bernard Dib John B Miller Peggy Bouzika Joan W Miller Demetrios G Vavvas Haijiang Lin |
author_sort |
Bo Tian |
title |
miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells. |
title_short |
miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells. |
title_full |
miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells. |
title_fullStr |
miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells. |
title_full_unstemmed |
miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells. |
title_sort |
mir-17-3p exacerbates oxidative damage in human retinal pigment epithelial cells. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2016-01-01 |
description |
Oxidative stress has been shown to contribute to the development of age-related macular degeneration (AMD). MicroRNAs (miRNA) are small non-coding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression. We showed miR-17-3p to be elevated in macular RPE cells from AMD patients and in ARPE-19 cells under oxidative stress. Transfection of miR-17-3p mimic in ARPE-19 induced cell death and exacerbated oxidative lethality that was alleviated by miR-17-3p inhibitor. The expression of antioxidant enzymes manganese superoxide dismutase (MnSOD) and thioredoxin reductase-2 (TrxR2) were suppressed by miR-17-3p mimic and reversed by miR-17-3p inhibitor. These results suggest miR-17-3p aggravates oxidative damage-induced cell death in human RPE cells, while miR-17-3p inhibitor acts as a potential protector against oxidative stress by regulating the expression of antioxidant enzymes. |
url |
http://europepmc.org/articles/PMC4978424?pdf=render |
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